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Rebecca McCullough, PhD

Assistant Professor, Department of Pharmaceutical Sciences

Mailing address:

The University of Colorado
Skaggs School of Pharmacy and Pharmaceutical Sciences
Department of Pharmaceutical Sciences
Mail Stop C238, Room V20-3128
12850 E. Montview Blvd
Aurora, CO 80045

Lab Location:

Pharmacy and Pharmaceutical Sciences Building (V20)
Third Floor, 3470D


Office: 303-724-6415
Lab: 303-724-4611
Affiliate Group: Alcohol Research Program

Training and Education:

  • Research Associate: Inflammation and Immunity, Cleveland Clinic
  • Postdoctoral Fellowship: Inflammation and Immunity, Cleveland Clinic
  • PhD: Toxicology, University of Colorado Anschutz Medical Campus
  • BS: Biology and Chemistry, Northern State University

Research Interests:

The major goals of our laboratory aim to better understand how chronic inflammation contributes to tissue injury following environmental exposures. Research in our lab is focused on these major areas:

Failed resolution of inflammation as a driver of alcohol-related liver disease (ALD)

In the past decades, alcohol-related morbidity and mortality has remained constant while the long-term prognosis for patients remains poor. ALD is multifactorial, mediated in part, by the innate immune system. More importantly, chronic inflammation resulting from chronic alcohol abuse contributes to hepatic as well as extrahepatic tissue injury via impaired resolution of the inflammatory response. The major goals of our lab are to better understand the mechanisms underlying the resolution of inflammation in chronic diseases associated with alcohol exposure and also targeting the resolution phase using cell-based immunotherapies as a potential treatment for individuals with ALD.

Adipose-liver crosstalk in metabolic diseases

There is a growing appreciation that extrahepatic organs, including adipose tissue, contribute to alcohol- and non-alcohol-related liver disease progression, but the mechanisms driving pathogenic organ-organ crosstalk are not well understood. Importantly, adipose inflammation is associated with multiple metabolic liver disorders. A growing research interest in our lab is determining how complement, a component of the innate immune system, drives pathogenic liver disease via modulation of the adipose secretome, including both soluble and extracellular vesicle (EV)-laden mediators including cytokines, chemokines, adipokines and microRNAs. Limited therapies exist for individuals with chronic liver diseases; a better understanding of intra- and inter-organ crosstalk may reveal potential therapeutic targets.


  • P2/P3 Seminar Research course
  • Toxicology Graduate Progam Curriculum